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A hepatitis C virus-encoded, nonstructural protein (NS3) triggers dysfunction and apoptosis in lymphocytes: role of NADPH oxidase-derived oxygen radicals

Artikel i vetenskaplig tidskrift
Författare Fredrik Bergh Thorén
Ana Romero
Magnus Lindh
Claes Dahlgren
Kristoffer Hellstrand
Publicerad i Journal of leukocyte biology
Volym 76
Nummer/häfte 6
Sidor 1180-6
ISSN 0741-5400 (Print)
Publiceringsår 2004
Publicerad vid Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning
Institutionen för laboratoriemedicin, Avdelningen för klinisk virologi
Sidor 1180-6
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Apoptosis/*immunology, Cell Communication/immunology, Cell Separation, Cytotoxicity Tests, Immunologic, Enzyme Inhibitors/pharmacology, Hepacivirus/immunology/*metabolism, Humans, Immune Tolerance/immunology, Killer Cells, Natural/drug effects/immunology/metabolism, Lymphocytes/*drug effects/immunology/metabolism, NADPH Oxidase/antagonists & inhibitors/*metabolism, Oxidative Stress/immunology, Phagocytes/metabolism/secretion, Reactive Oxygen Species/*metabolism, T-Lymphocytes/drug effects/immunology/metabolism, Viral Nonstructural Proteins/*pharmacology
Ämneskategorier Immunologi inom det medicinska området

Sammanfattning

The persistent infection caused by hepatitis C virus (HCV) is presumably explained by a deficient immune response to the infection, but the basis for the inefficiency of immune-mediated virus eradication is not known in detail. This study addresses mechanisms of relevance to dysfunction of cytotoxic lymphocytes in HCV infection, with a focus on the role of phagocyte-derived oxygen radicals. We show that NS3, a nonstructural, HCV-encoded protein, induces a prolonged release of oxygen radicals from mononuclear and polymorphnuclear phagocytes by activating a key enzyme in radical formation, the reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. The NS3-activated phagocytes, in turn, induced dysfunction and/or apoptosis in three major subsets of lymphocytes of relevance to defense against HCV infection: CD3+/56- T cells, CD3-/56+ natural killer (NK) cells, and CD3+/56+ NKT cells. Two inhibitors of the NADPH oxidase, histamine and diphenylene iodonium, suppressed the NS3-induced oxygen radical production and efficiently protected lymphocytes against NS3-induced apoptosis and dysfunction. In conclusion, we propose that NS3, by triggering oxygen radical formation in phagocytes, may contribute to the dysfunction of antiviral lymphocytes in HCV-infected liver tissue and that strategies to circumvent oxidative stress may be useful in preventing HCV-associated carcinogenesis and facilitating lymphocyte-mediated clearance of infected cells.

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